14 - Ischaemia, infarction and shock Flashcards Preview

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Flashcards in 14 - Ischaemia, infarction and shock Deck (33):
1

Why is reperfusion of non-infarcted but ischaemic tissues not always good?

Generation of reactive oxygen species by inflammatory cells causes further cell damage === reperfusion injury

2

Main causes of infarctions

Thrombosis and embolism

3

Other causes of infarctions

vasopasm
artheroma expansion
extrinsic compression
twisting of vessel roots (volvulus)
rupture of vascular supply (AAA)

4

Infarction morphology

Red (haemorrhagic)
White (anaemic)

5

what necrosis in the brain

colliquative

6

most popular necrosis

coagulative

7

if someone dies of a sudden heart attack what histology do you see?

nothing! as no time to develop haemorrhage / inflammatory response

8

factors affecting the degree of ischaemic damage

nature of the blood supply
rate of occlusion
tissue vulnerability to hypoxia
blood o2 content

9

most vulnerable organs for infarction

kidneys, spleen, testis

10

a slow rate of occlusion makes you more or less likely to have an infarct?

less likely as it allows development of collateral perfusion pathways

11

blood oxygen content

anaemia increases chance of infarction

congestive heart failure - poor CO and impaired pulm. vent. may develop an infarct with normally inconsequential narrowing of the vessels

12

shock definition

physiological state characterised by significant reduction of systemic tissue perfusion (severe hypotension) resulting in decreased O2 delivery to the tissues

13

shock's effects at a cellular level

Membrane ion pump dysfunction
Intracellular swelling
Leakage of intracellular contents into the extracellular space
Inadequate regulation of intracellular pH
Anaerobic resp --> lactic acid

14

shock's effects at a systemic level

Alterations in the serum pH (acidaemia)
Endothelial dysfunction -> vascular leakage
Stimulation of inflammatory and anti-inflammatory cascades
End-organ damage (ischaemia)

15

Shock and reversibility

Shock is initially reversible but rapidly becomes irreversible

16

Result of shock

Cell death
End-organ damage
Multi-organ failure
Death

17

Classification of shock

Hypovolaemic
Cardiogenic
Distributive

18

Types of distributive shock

Anaphylactic
Septic
Toxic shock syndrome
Neurogenic

19

Hypovolaemic shock

Intra-vascular fluid loss (blood, plasma etc)
Decrease in venous return to heart aka pre-load
Lower stroke volume therefore low CO

20

How to compensate for hypovolaemic shock

Increase blood volume

21

Causes of hypovolaemic shock

Haemorrhage - trauma, GI, rupture, fractures, aneurysm rupture

Non-haemorrhagic - diarrhoea, vomiting, heat stroke, burns

Third spacing

22

What is third spacing?

Acute loss of fluid into internal body cavities

Third-space losses are common post-op and in GI obstruction, pancreatitis or cirrhosis

23

Cardiogenic shock - why? how to compensate?

Cardiac pump failure with low CO
How to compensate -> increase in systemic vascular resistance

24

Causes of cardiogenic shock

Myopathic (heart muscle failure)
Arrythmia related
Mechanical
Extra cardiac (obstruction to blood flow)

25

Extra cardiac cardiogenic shock e.g.s

Anything that impairs cardiac filling or ejection of blood from heart

Massive PE, tension PT, severe constrictive pericarditis, pericardial tamponade

26

Distributive shock

Decrease in systemic vascular resistance due to severe vasodilation

Compensate via increasing CO

27

Septic shock which organisms? who's at risk? pathophysiogical features

Gram +ve, -ve bacteria or fungi and affects immunocompromised, elderly, very young

Increase in cytokines/mediators leading to vasodilation

Pro-coagulation (DIC)

28

Anaphylactic shock - pathophysiology

Severe type I hypersensitivity rxn

Small doses of allergen = IgE cross-linking

Massive mast cell degranulation which = vasodilation

29

Anaphylactic shock - body's rxn

Contraction of bronchioles/ resp. distress

Laryngeal oedema
Circulatory collapse -> shock/death

30

Neurogenic shock

Spinal injury / anaesthetic accidents = loss of sympathetic vascular tone

Vasodilation -> shock

31

Toxic shock syndrome

NOT SAME AS SEPTIC SHOCK

32

Toxic shock syndrome - causative organism

S. aureus
S. pyogenes

33

Toxic shock syndrome - pathophysiology

do not require processing by APCs

non-specific binding of MHC II to T cell receptors with up to 20% of T cells being activated at once

Widespread cytokine release = decrease in SVR